An intelligent fuzzy-based emergency alert generation for persons with episodic memory decline problems

Many humans deal with problems that concern episodic memory decline. These problems can cause annoying, and sometimes, dangerous incidents, like failing to recall the name of a friend or forgetting to take a medicine or turn off the cooker. Concerning the above, this paper presents a fuzzy rule-based mechanism that generates emergency alerts when a dangerous situation is caused by an inconsistency in the human’s actions in the home environment. In such a way, the system protects persons with episodic memory decline problems or lapses of attention from dangerous situations that may be caused by their memory disorder and allows them to complete an everyday activity. For the paper’s needs the application of the presented mechanism is limited to the usage of a cooker. The system takes as input the time, the size and the content of the pot that is used to the cooker, calculates the degree of emergency and describes it using fuzzy sets and, finally, applies rules over the fuzzy sets to generate alert messages that notify the monitored person about the next action that s/he has to do in order to complete a particular activity. For the evaluation of the system, we have developed a simulation program that asks users to complete some activities during a specific time period. The system embeds the presented fuzzy rule-based mechanism and monitors the user’s actions and generated alerts, which concern the usage of the stove burner. The simulation software was used by 15 users. Their reactions and opinions about the system’s alerts and the assistance it offers, are positive.

Rehabilitation organisch bedingter Gedächtnisstörungen: Was, wann, für welche Betroffenen?

The aim of this paper is to provide an overview of treatment strategies and methods as well as a practical decision support, based on the current version of the guideline on memory rehabilitation [55] and the authorsʼ views. We show that the choice of a method for efficient neuropsychological treatment depends on the type and severity of the memory disorder as well as on the previous therapy experience of the affected person and the defined therapy goal: e.g., what it means to work with implicit »errorless learning« methods; which form of external memory aids can be used with which patients; that methods for improving memory performance are available for persons with moderate to mild memory disorders; and that PC therapy is also likely to help younger and more mildly affected persons. The aim is also to provide a broad overview of current studies on memory rehabilitation, some with very promising results. However, many questions remain unanswered to date, some of which have been highlighted in this paper with the aim of stimulating future research to enable those affected by memory impairment to achieve the best possible rehabilitation and the greatest possible independence

Macrophage- and Microglia-Related Chemokines Are Associated with Small Vessel (White Matter) Vascular Dementia: A Case-Control Study

<b><i>Introduction:</i></b> Little is known about the role of inflammation in the process of small vessel vascular dementia (VaD). Recently, the notion that small vessel VaD is caused solely by vascular pathology has been challenged by new evidence of concomitant breakdown of the blood-brain barrier and dysregulation of neuroinflammation in the white matter. <b><i>Methods:</i></b> We examined selected inflammatory cytokines and chemokines in the plasma from patients with small vessel VaD (<i>n</i> = 41) and from age-matched controls (<i>n</i> = 131) using multiplex bead-based assays. Participants were recruited from a memory disorder clinic and from a hospital or community. <b><i>Results:</i></b> When compared to controls, patients with small vessel VaD had a highly significant increase in the plasma interferon-γ-inducible protein 10 (IP-10) level (<i>p</i> &#x3c; 0.0001) and a highly significant decrease in plasma macrophage inflammatory protein 1-beta (MIP-1β) level (<i>p</i> &#x3c; 0.0001). We also observed a significant increase in patients’ levels of interleukin-10 (IL-10) (<i>p</i> = 0.022) as well as decreases in interleukin-8 (IL-8) (<i>p</i> = 0.004) and interleukin-7 (IL-7) (<i>p</i> = 0.011) when compared to age-matched controls. <b><i>Conclusion:</i></b> Both IP-10 and MIP-1β are macrophage-related chemokines. The significant differences between cases and controls suggest a potential role for macrophages in small vessel VaD neuroinflammation. Although it remains unclear whether there is a causal effect of their alteration for small vessel VaD, a better understanding of these molecules in the pathogenesis of small vessel VaD may lead to improved diagnosis and future treatment outcomes against this disease.

Assessment of the effects of maternal deprivation in offspring treated with ultra-high diluted Zincum metallicum in rats

Introduction: Clinical studies have shown that adverse events in childhood can lead to the development of psychiatric disorders, such as anxiety, in adolescence and adulthood in humans. Manipulations with laboratory animals, such as maternal deprivation (MD), are a source of stress for the offspring and can be a useful tool for the understanding how these events in the early period of development can lead to behavioral changes in adulthood. Studies about the use of homeopathic ultra-high dilutions as tools to minimize stress are found in the literature, i.e. Zincum metallicum is used for the treatment of neurological and behavioral symptoms, including: weakening of intellectual functions with brain and nervous exhaustion, loss of vitality, slow comprehension, memory disorder, general tremor and constant movements. These alterations can be characterized as stress-related phenomena in different species. Aim: The aim of this study was to evaluate the long-term effects of homeopathic treatment in animals subjected to stress in their early days (maternal deprivation). This study was approved by the Ethics Committee of the University of Santo Amaro (UNISA), according to Process number 11/2014. Materials and Methods: In this study, newborn female rats were subjected to maternal deprivation and treated from the 10th day of lactation (PND10) until weaning (PND21). The animals were divided in 4 groups: 8 treated with Zincum metallicum 30 cH (Zn30cH); 8 treated with Zincum metallicum 6 cH (Zn6cH); 8 treated with 10% hydroalcoholic solution (medicines in blind trials, identified by codes); and 8 animals who had neither taken anything (“blank control”) nor experienced deprivation. The animals were weighed weekly, from weaning until the end of the experiment, and evaluated in the Open Field (OF) and in the Plus Maze (PM) devices to measure mobility, emotionality and anxiety, in 3 moments: in PND21 (childhood), during puberty (PND 40) and adulthood (PND75). Data were analyzed statistically by ANOVA, followed by the Bartlett's Test and Bonferroni's Multiple Comparison Test, being p≤0.05. Results and Discussion: In the OF, it was observed reduction of immobility in Zn6cH group (p≤0.05) at PND21. At PND40, the Zn30cH group showed higher activity than the other groups, with increased rearing and decreased immobility (p≤0.05). Finely, at PND75 (adulthood) no change occurred, and Zincum metallicum treated rats presented similar behavior to the undeprived animals. In the PM, at PND21, the Zn30cH treated deprived group showed decrease in the open arm entry and retention period in the Maze, compared to the control undeprived group (p≤0.05). The time in the closed arm was higher than the undeprived control group and the number of head dips was lower (p≤0.05). The PM observation at 45 and 75 days showed no statistical difference among groups. The deprived animals which took Zn30cH obtained the same gain that the undeprived animals did (p≤0.05). Therefore, the deprived animals that presented anxiety during childhood were in accordance to other studies, showing that maternal deprivation is a stress factor that causes anxiety. However, the time of emotional unbalance was shorter in rats treated with Zincum metallicum. Conclusion: Zincum metallicum 30 cH seems to be a potential medicine to manage troubles in the childhood derived from stress caused by maternal deprivation. However, other studies are already underway with male offspring and neurochemical measurements, for a better parameter of results.

Horse Placental Extract Enhances Neurogenesis in the Presence of Amyloid β

Human placental extract and animal-derived placental extracts from pigs and horses host a wide range of biological activities. Several placental products are used as medicines, cosmetics, and healthcare substances worldwide. However, the use of placental extracts for neuronal functioning is currently not established because the number of relevant studies is limited. A few previous reports suggested the neuroprotective effect and dendrite genesis effect of placental extract. However, no studies have reported on neurogenesis in placental extracts. Therefore, we aimed to investigate the effects of horse placental extract on neurogenesis, and we examined the protective effect of the extract on the onset of memory disorder. A horse placental extract, JBP-F-02, was used in this study. JBP-F-02 treatment dose-dependently increased the number of neural stem cells and dendrite length under Aβ treatment in primary cultured cortical cells. The oral administration of JBP-F-02 to a 5XFAD mouse model of Alzheimer’s disease at a young age significantly prevented the onset of memory dysfunction. This study suggests that the extract has the potential to prevent dementia.

Molecular Mechanism of ATF6α/S1P/S2P Signaling Pathway in Hippocampal Neuron Apoptosis in SPS Rats

Apoptosis of hippocampal neurons is one of the mechanisms of hippocampal atrophy in posttraumatic stress disorder (PTSD), and it is also one of the important reasons of memory disorder in PTSD patients. The endoplasmic reticulum stress (ERS) mediated by activated transcription factor 6α(ATF6α)/site 1 protease (S1P)/S2P is involved in cell apoptosis, but it is not clear whether it is involved in hippocampal neuron apoptosis caused by PTSD. The PTSD rat model was constructed by the single-prolonged stress (SPS) method. The experiment was divided into two parts: (1) Control group, SPS 1d group, SPS 7d group, SPS 14d group. (2) Control group, SPS 7d group, SPS 7d+AEBSF group, control+AEBSF group. 4-(2-Aminoethyl) benzenesulfonyl fluoride hydrochloride (AEBSF) is an ATF6α pathway inhibitor. The expression of ATF6α, glucose regulated protein (GRP78), S1P, S2, C/EBP homologous protein (CHOP), caspase-12 protein and mRNA in the hippocampus of PTSD rats were detected by immunohistochemistry, Western blotting and qRT-PCR. The apoptosis of hippocampal neurons was detected by TUNEL staining. In experiment 1, the protein and mRNA expression of ATF6α, GRP78 increased gradually in SPS 1d group and SPS 7d group, but decreased in SPS 14d group(P<0.01). In experiment 2, compared with the control group, the protein and mRNA expression of ATF6α, GRP78, S1P, S2P, CHOP, caspase-12 and apoptosis rate were significantly increased in SPS 7d group(P<0.01). However, the protein and mRNA expression of ATF6α, GRP78, S1P, S2P, CHOP, caspase-12 and apoptosis rate were significantly decreased after AEBSF pretreatment(P<0.01). SPS induces apoptosis of hippocampal neurons by activating ERS mediated by ATF6α, suggesting that ERS-induced apoptosis is involved in the occurrence of PTSD.

The frequency and framing of cognitive lapses in healthy adults

Objective Many people present to health services with concern about cognitive symptoms. In a significant proportion those symptoms are not the result of pathologically defined brain disease. In some they are part of a functional cognitive disorder (FCD). We assessed the frequency of cognitive lapses in a non-clinical sample in order to consider the utility of frequency of cognitive lapses in diagnosing cognitive disorders. Methods Healthy adults, who had never sought help for cognitive symptoms, completed a questionnaire, distributed via social media, about self-evaluation of cognitive function, frequency of cognitive lapses, and use of memory aids, including Schmitdke and Metternich’s functional memory disorder (FMD) inventory. Results One hundred and twenty-four adults, aged 18–59 (median 23), most with further or higher education, responded. Thirty-one (25%) reported “fair” or “poor” memory. Forty-eight (39%) reported memory worse than 5 years ago, and 30 (24%) reported memory worse than others the same age. Participants endorsed a mean 13/18 specific cognitive lapses at least monthly. One hundred and eleven (89%) scored ≥4, the suggested cutoff for the FMD inventory. Conclusions Cognitive lapses described in FCDs are common in highly educated adults. The high frequency of lapses in this healthy population suggests self-reported frequency of lapses alone cannot discriminate FCDs from “normal” experiences. Further research is required to clarify the role of abnormal metacognition in FCD. Better understanding of the factors moderating subjective interpretation of cognitive failures will also aid development of better clinical risk-stratification methods in people concerned about future dementia.